作者
樊 宇,杨历新
文章摘要
目的:在代谢性心血管疾病(CVD)负担上升背景下,阐明低氧作为“代谢—血管”轴共同上游病因的证据链。方法:系统梳理脂肪组织低氧、阻塞性睡眠呼吸暂停所致间歇性低氧(IH)以及内皮代谢重编程/铁死亡的基础、转化与临床研究,并综合干预证据。结果:三类低氧表型可并存并相互放大:脂肪组织低氧驱动炎症与胰岛素抵抗,IH通过交感与氧化炎症应激加重代谢紊乱和内皮功能障碍,铁死亡参与微血管病变的终端环节。减重+运动(含低氧训练)+优化CPAP,联用降脂及SGLT2抑制剂等可实现多点拦截。结论:以TyG、ODI及脂过氧化/铁代谢面板进行分层评估,联动依从性指标,有望明确“低氧减负”与代谢—血管获益的因果通路,支撑个体化干预。
文章关键词
低氧;间歇性低氧;代谢性心血管疾病;脂肪组织;内皮功能;铁死亡;HIF
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